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91 Cards in this Set

  • Front
  • Back
T/F the PA is larger than the aorta in teh neonate?
Fetal hemoglobin is at best __% saturated?

Adult's best and worst saturation
Fetal - 70% at best

Adult - 100% (best) - 75% (worst)
In normal fetal circulation, how much blood flows through the PA?
7% of total CO

-lungs arent fxnal so they only need enough blood to support growth
What causes high in utero pulmonary resistance?
Pulmonary arteriole constiction
Prenatal pressure generated by R Ventricle?

L Ventricle?
50-70 mmHg for both R & L (generate same pressure prenatally)
At what point does pulmonary resistance drop?
Sudden drop at birth and a continuous drop for 3-6 weeks afterwards
What are the 3 mechanisms by which pulmonary vascular restance drops at birth? time span?
1) Mechanical - take first breath of air -> expansion (immediate)

2) Biochemical - ^ PaO2 makes pulmonary arteries dilate (seconds to hours)

3) Remodeling - loss of smooth muscles in arterioles (3-6 weeks)
Acidosis does what to the DA? O2's effect?
Both acidosis and vPaO2 makes it remain patent & do the OPPOSITE for the Pulmonary arterioles (open w/ ^PaO2, etc)
Drugs that cause the DA to close and remain patent?

Pulmonary arterioles?
PGE1 (prostaglandin) - open DA

Indomethacin (NSAID - close DA

NO causes dilation of pul arterioles
Condition where the resistance to blood-flow in the lungs doesn't change appropriately in newborns?

Causes (5)?
Persistent pulmonary HTN of the newborn

1)Meconium (sticky,green stool) sucked into the small airways with the first breath

2)Not enough O2 saturation

3)Patent DA

4)Patent FO

5)Pulmonary arterioles remain constricted
Treatment for persistent pulmonary HTN of newborn (6)?


3)Bicarb (treat acidosis)


5)Paralytics - v O2 demand

6)EMCO - extracorporeal membrane oxygenation (used in heart surgery); worst case scenerio

-dont close the DA because the resistance in the lungs may be high, causing CO to stop
Patent DA ultimately causes what?

Acutely (3)

Physical presentation?
Ultimately CHF (BIG DA)

Acutely (SMALL DA)..

1)Respiatory distresss syndrome (aka hyaline membrane disease) - severe pulmonary edema

2) L to R shunt

3) LV volume overload

Initially pink, become blue for 2-3 day, get better, then when DA becomes a problem have tachypnea and dyspnea
2 ways to non-pharmacological ways to treat PDA?
1) Embolization coil - lasso the DA (SMALL DAs)

2) Amplatzer Ductal Occluder - burn DA with cage/top hat thing made of Nitinol fibers (BIG DAs)
Cause of small/poorly developed aorta?
Hypoplastic LV


-do well prenately b/c O2 coming from placenta
DA closure normally occurs how long after birth?
72 hours

-with patent FO, baby does well until then

ie baby given birth, fed, not monitored for a couple hours -> can become acidotic and die

-need to give PGE1!
4 Steps/Procedures of Fontane Circulation for Hypoplastic Left Heart
STAGE 1 (Norwood procedure) - a)connect PA and aorta (gortex shunt), b)atrial septectomy

STAGE 2: 6 months, big head/little body; bidirectional Glenn shunt - plug SVC into PA

STAGE 3: ~2 years of age; plug IVC into the PA (taking R atrium out of circulation)
4 parts to the Tetralogy of Fallot

How to treat
1)Pulmonary Stenosis

2)R Ventricular hypertrophy


4)Overriding aorta

-Babies do okay prenatally

-Once born MAINTAIN patent DA, then replace with shunt when inefficient

-As baby grows, patch up VSD an open up PA (relieve obstruction)

-Might later have a valved put in as adult to prevent from pulmonary regurgitation
Most common congential heart defect?
What determines the shunt in a VSD (2)?
1)Size of the hole/defect (if small enough then there can still be a pressure difference)

2)Resistance downstream

-not determined by the pressure generated by the heart muscles
What happens if VSD too large?
Loss of pressure difference b/w ventricles

-lung arteries stiff from overcirculation (resistance) -> pumping too much blood with their L ventricle (tachypnea and gallop)

-major problem is CACHECTIA b/c its hard to drink when youre breathing hard

-usually closed with Dacron patch
What size hole in VSD makes the noisiest murmurs?
MEDIUM sized holes

-small VSD dont have enough blood cells going through hole to carry much energy to wall and rattle it
Do VSD cause AV block?
No, typical musclar VSD are far from the conduction system
Eisenmenger's syndrome
Irreversible pulmonary vascular changes due to increased flow and pressure causing blood flow to go from R to L

-unlike most big VSDs patients dont quite get sick enough to have failure to thrive and DONT have murmur (so dont pick up until damage to lung is too great)
Summary of VSD
Tiny ones go away on their own

Big ones have heart failure

Medium ones make noise and worry you (some fix by themselves, some dont)

Eisenmenger's VSD go backwards b/c of pulmonary congestoion
Fixed splitting?
ASD has what distinguishing heart sounds (2)?
1) fixed splitting

2) systolic murmur b/c of RV overload (due to RA being more compliant than LA)

What catastrophic event may arise from ASD?
Paradoxical embolism

-also have conduction system abnormalities (but not with VSD)
Worst congenital heart lesion of all?
A-V canal Defect aka Endocardial Cushion Defect


A-V canal defect most common in
Down Syndrome patients
How to fix Transposition of the Great arteries (3)?
1) Prostaglandins for patent DA/oxigentation or create foramen ovale by tearing hole/oxigenation

2)Senning operation - rerouting the PULMONARY venous and arterial flow - RV = system venticle (dysfxn over lifetime)

3)ARTERIAL Switch operation - two big vessels are cut just over valves and switched (also have to maticulously switch respective coronary arteries) - MUST BE DONE IN NEONATAL PERIOD
Total Anomalous pulmonary venous return problem? Corrections?
Pulmonary veins come together in the confluence BEHIND the heart (not inside it) -> goes to RA instead of LA

Must have ASD to survive

Corrected by sewing PV back onto LA; one of best cardiac heart diseases to have b/c you havn't cut much if any of the heart and everything is normal
Way to detect Tricuspid Atresia
Cyanosis, always desaturaed because of mixing leasion

Very unusual EKG w/o heart block (but do have conduction system abnormalities)

Always find with ASD (or VSD?)..must have to survive
Another congenital heart defect that presents with early cyanosis
Truncus Arteriosus

-MAKES MURMUR right away...hard to miss

-Fixed by patching the VSD, putting in a tube and then valves

-different b/c NO VALVES placed early on for T of Fallot
Sudden loss of consciousness and postural tone caused by DIMINISHED CEREBRAL BLOOD FLOW

-causes are rarely neurologic...mostly CARDIAC CASES
How long decreased blood flow to brain before LOC in syncope

Main variable factor in determining amount of time?
6 seconds (only 4 in elderly)
-espcially if standing

POSTURE is main factore...can have asystole for a longer period if in supine position
Three signaling causes of syncope?
1) Vertigo - false sense of motion/spinning

2) Unsteadiness - difficulty w/ balance - usually NEUROLOGIC

3) Faintness ("presyncope)
Vertigo is a disorder of ? Causes?
Vestibular system

Causes include:

-Acute labyrinthitis - usually caused by VIRAL infection

-TIA (Transient Ischemic Attack) or stroke involving the BRAINSTEM

-Schwannoma of CN VIII ("Acoustic Neuroma) - begign neoplasm
Orthostatic Hypotension
dramatic drop in systolic BP after sitting up or standing too quickly; causes presyncope (faintness) usually
Causes of postrual syncope (4)
1) Orthostatic Hypotension - Fall in BP upon standing

2) Acute volume loss - GI bleeding, excessive sweating, nausea, vomiting, diarrhea

3) Loss of neurologic tone - usually of ANS - Diabetic peripheral neuropathy, Shy-Drager syndrome (progressive degenerative dz of ANS)

4) Medication (MCC!!) - antihypertensive/diureic use (alpha methyl dopa, clonidine, any antihypertensive)
MCC of syncope?

Arises from?

Vasovagal syncope

-Situaltional event stimulated vagal and withdrawing SNS tone (ie extreme EMOTION, painful/unpleaseant stimuli)

-Prolonged pauses b/w sequential HB's (seeing on EKG)

-History of passing out thoughout lifetime

-NASEA usually involved

-MEN > women`
Common Syncope cause found in old men?
Carotid Sinus Hypersensiivity

-overactivity of the carotid sinus (reflex = vasodilation; afferent arc - CN IX, efferent arc - CN X)
2 other Autonomic causes of syncope
1) Glossopharyngeal neuralgia

-syncope w/ swallowing stimulation of aff CNIX upon swallowing stimulates CN X to give reflex output (pass out)


2) Spinal Cord Injury
-usually C5 or higher, poor prognosis
Key to Cardiac Syncope
SUDDEN onset, SUDDEN offset

-w/out warning!
-history of cardiac disease is common

-therefore, whenever you have a patient w/ cardiac history and syncope, send to cardiologist immediately

-potentially LETHAL
Patterns of syncope w/ exercise?
Syncope DURING exercise is BAD (very malignant - often ventricular fibrillation)

Syncope AFTER exercise is OKAY (benign, usually vasovagal)
Causes of cardiac syncope (3)?
1) Heart rate too fast (tachy)

2) Heart rate too slow (brady)

3) Obstruction to blood flow
Two main causes of bradycardia?
1) SA node dysfunction (MCC!! High prevalence in *OLD people*)

2) AV block

-sometimes BOTH!
Lack of P wave and absence of following QRS complex?

SA Node dysfxn

digoxin, beta blockers, calcium blockers

-RARELY the cause fo suden death

Tx - withdraw of aggravating medicine + surgically implant permanent pacemaker
Bradycardia OR long pause AFTER teremination of Atrial Fibrillation/Atrial Flutter
Tachycardia-Badycardia Syndrome
PR interval is prolonged (>200 ms)
Primary AV Block

-usuallly asymptomatic
BBB w/ consistent PR interval and wide QRS

What is the usual P:QRS conduction ratio?
Mobitz II Secondary AV Block

-poor prognosis, ALWAYS requires permanent pacemaker

3:2 P:QRS conduction ratio
Progressive PR interval prolongation until atrial deloarization is dissociated from ventricular depolarization
Mobitz I Secondary AV Block (Wenckeback Block)

-QRS narrow b/c block is NOT in BB (it's in the AV Node)

-if symptomatic, requires pacemaker
Complete AV dissociation w/ narrow QRS
Tertiary AV Block in AV Node

-no conduction and no syncrony of P wave with QRS wave

-if symptomatic, which it almost always is, requires pacemaker
Complete AV dissociation w/ wide QRS
Tertiary AV Block in Bundle Branches

ALWAYS requires pacemaker
Sawtooth waves

What leads?

Atrial Flutter
-a regular rhythm

-sawtooth leads in leads II, III, aVF

-Catheter ablation in the right atrium to stop re-entrant rhythm around the tricuspid valve
Most common (MC) sustained arrhythmia
Atrial Fibrillation

Tx: Slow the AV nodal conduction
MC regular narrow complex tachycardia
AV NODAL Reciprocating Tachycardia (re-enters through AV node)

not..wideQRS-AV Reciprocating Tachycardia which is associated with W-P-W syndrome (BBB - reenters, bypassing AVnode of atrial and taking accessory pathway; this bypass eliminates teh AV node delay and shortens PR interval)

-both commonly associated with syncope
AV Nodal reciprocating Tachycardia more common in men or women?
Delta wave think
Wolff-Parkinson-White Syndrome

D wave = slurred upstoke in QRS complex that is associated with short PR interval (thanks wiki!)

-HR > 300 bpm!!

-has a wideQRS-AV Reciprocating Tachycaria (reentry through accessory pathway (Bundle of Kent), see 2 questions prior)

-may result in SUDDEN DEATH
Most lethal of all causes of syncope
Ventricular Tachyarrhythmias

-medical emergency - syncope/sudden death!

-NEED implantable cardioverter-defibrillator (ICD)
Common final pathway for all forms of Sudden Cardiac Death (SCD)

SCD accounts for what % of all cardiac related deaths in US?
Ventricular fibrillation
-requrires a defibrillator

At __ minutes, 90% of patiens will be in VF?
At EMS arrival, if patient is found still in ___ as compared to ___, their chances for successful resuscitation are still high
VF as compared to asystole, chances for survival are better
Most important factor for survival in SCD is?
Time to Defibrillation

CPR initiated < 3min after syncope, then defibrillate - survival ^ to 70%

without CPR, survival drops below 40%
Placement of + & - pads of defibrillator
+ pole = sinus

- pole = apex

electrical flow from + to -
Rhythm related to long QT interval
Torsades de Pointes VT
-special form of VT

-CONGENTITAL disorder of Na or Ca channels (KIDS)
-OR DRUG induced (ADULTS)

-or electrolyte disturbances (esp hypokalemia or hypomagnesemia)
MCC of Sudden Death in Young MEN from SOUTHEAST ASIA
Brugada syndrome

mean age of sudden dean is 33
RBBB, ST elevation V1-V3

T wave inversion seen in V2 leads
Brugada syndrome
Patient with Idiopathic Ventricular Tachya's and run of premature ventricular contractions with syncope but usually not sudden death

-this was the best i could come up...
Benign ventricular tachycardia
Classic story of syncope during physical exertion, you should think...

Common Causes?
Obstructivce Cardiac Syncope

Blood flow is not getting out of the heart:
-Aortic Stenosis
-Hypertrophic obstructive cardiomyopathy
-Coronary artery Dz - usually L amin coonary artery stenosis
-Pulmonary HTN
Sys of more than 120 in LV, think...
aortic stenosis
How can you estimate the severity of a mitral valve stenosis
Gradient b/w the wedge pressure and the LV diastolic pressue

15 - severe

10 - moderate

5 - mild
Any patient that sometimes ahs normal BP, and sometimes has realy high BP (espsciallly depending on the position of the body of exercise) think...
Epinephrine Secreting pheochromocytoma symptoms?

Epi: Flashing, HA, palpitations

NE: asymptomatic hypertension
Carey-Coombs murmurs
Mirtral stenosis during acute rheumatic fever
Calcification in aortic stenosis always occurs where?
Aortic side
Calicified pulmonary stenosis is ?
a congenital problem

-affects YOUNG people not old
Everytime you have syncope in times of exercise problem always points to ?
-fast-on, fast-off

and is always very threatening
Neck vein collapse w/ hepatojugular reflex & peripheral edema
R Heart Failure
Hepatojugular reflex
compress the liver -> jugular vein becomes much more distended
Murmur propagates to carotid artery?
Aortic stenosis - "bouncing pulses"

also have S4 b/c of less compliant left ventricle
Short diastolic murmur
Aortic regurgitation

- flutter of anterior leavlet of mitral valve
Single S2 sound probably
Stenotic, CALCIFIED aortic valve (aortic side only remember!), which doesnt make noise when it closes

-probably just hearing P2 (while calcified A2 remains silent)
Only treatment for congenital bicuspid valves (have lots of calcification)?
Replacing the valve
T/F Mild aortic regurgitation is common with aortic stenosis

"if you have difficulty opening, then you'll have difficulty closing as well"
Midsystolic click followed by high pitch rescendo-decrescendo murmur that occupies second half of systole without masking 2nd sound
Mitral valve prolapse
Murmur transmitted to axilla
PROLAPSE of ANTERIOR leaflet of mitral valve
Murmur transmitted to middle of the precordium
PROLAPSE of POSTERIOR leaflet of mitral valve

-posterior leaflet invovlemnet is more common than the anterior leaflet
'P' Mitrale means

...not sure about this questions...correct me if im wrong
P wave is amplified, especially in V1, V2, V3

Common in MV prolapse
As L Atrium increases in size...more prone to develop?
Atrial fibrillation (and flutter, maybe?...not sure)
Right sised bacterial endocarditis presentation?
IV drug users

Hemorrhage under the nails clear sign for?